DOCSLIB.ORG

© 2021 Reachmd Page 1 of 5

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
© 2021 Reachmd Page 1 of 5 Transcriipt Detaiills This is a transcript of an educational program accessible on the ReachMD network. Details about the program and additional media formats for the program are accessible by visiting: https://reachmd.com/programs/clinicians-roundtable/antidepressants-the-lay-of-the- land/3346/ ReachMD www.reachmd.com [email protected] (866) 423-7849 Antidepressants: The Lay of the Land ANTIDEPRESSANTS: THE LAY OF THE LAND Regardlless of your speciiallty, Prozac, Zolloft, and Paxiill have become commonlly used and famiilliiar mediicatiions. What others shoulld we know? You are lliisteniing to ReachMD, The Channell for Mediicall Professiionalls. Wellcome to the Clliiniiciian''s Roundtablle. I am Dr. Leslliie Lundt, your host, and wiith me today iis Dr. Stephen M Stahll. Dr. Stahll iis Adjjunct Professor of Psychiiatry at the Uniiversiity of Calliiforniia iin San Diiego. He iis an iinternatiionalllly recogniized clliiniiciian, researcher, and teacher iin psychopharmacollogy and he has authored more than 350 artiiclles and chapters. Hiis llatest book iis the thiird ediitiion of Stahll''s Essentiiall Psychopharmacollogy. DR. LESLIE LUNDT: Welcome to ReachMD, Dr. Stahl. DR. STEPHEN M. STAHL: My pleasure to be here. DR. LESLIE LUNDT: How do you currently explain how antidepressants work in the brain. We have all seen these little commercials put out by the pharma companies with a little blob. I am wondering if that's really how they work? DR. STEPHEN M. STAHL: Well, I think that we know where the antidepressants bind, but I am not sure that that means we know how they work. Certainly, if the blobs are monoamines that’s probably the best bet we have to explain these drugs right now. The monoamines particularly serotonin is the most famous and norepinephrine it's sister, but even dopamine. These 3 monoamines sometimes called trimonoamines are the targets of every known antidepressant, and in fact it's only in research that we have ever identified a non-monoaminergic kind of mechanism that ever worked for depression. So, the current antidepressants someway or another we think boost monoamine neurotransmission and that’s how they are thought to work in the brain. © 2021 ReachMD Page 1 of 5 DR. LESLIE LUNDT: Boost monoamine transmission, but what kind of timeframe, clearly they don’t work right away. DR. STEPHEN M. STAHL: That’s good question. Indeed they do not work right away. It turns out that if you block a monoamine transporter that is an inactivator of a monoamine, it will cause a buildup of the monoamines, but not a very big one even though it’s a very sudden one. In fact, it probably makes them buildup sufficiently to cause a side effect, but not a therapeutic effect. So what's happening? Well, if you sustain the buildup of the monoamines, the neuron will react by down regulating certain receptors. Those receptors are mostly, if you will, bricks, they turn off the release of monoamines. So if you down regulate them or you cut the brick cable, boom, you get a big amount of monoamines being released, so we think what happens is that the antidepressants suddenly block transporters, which then causes the monoamines to indirectly decrease, down regulate the bricks of the neuron, which then 70 days later something like that will cause a much more profound increase of the monoamines, so it's thought that that increase of the monoamines with a delay is what's necessary in order to exert an antidepressant effect. DR. LESLIE LUNDT: Besides the basic SSRIs as I mentioned sertraline, fluoxetine, paroxetine, what other antidepressants are important for our listeners to know? DR. STEPHEN M. STAHL: Well, they certainly are the SNRIs or serotonin-norepinephrine reuptake inhibitors also called dual action drugs and of course there are 3 almost 4 of them. The 3 that are out there are Effexor (venlafaxine) is the branded name and unbranded name, then there is (duloxetine) Cymbalta, but you also have the new one Pristiq, which is desvenlafaxine and one that's imminent to be approved at the FDA, but not for depression, but perhaps for fibromyalgia called milnacipram. Those are SNRIs. We also have Wellbutrin, which is kind of in a class by itself also called bupropion and it's a dopamine and norepinephrine reuptake inhibitor or NDRI if you will. Of course, you have got old-fashioned trazodone, you got the tricyclics, you got the old MAO inhibitors. I will put a little plug in here. If the listeners are psychopharmacologists of any sophistication is one of the secret weapons in the armamentarium for treatment resistance, but almost nobody prescribes them anymore. So they are the major classes. The mirtazapine is a interesting drug. Remeron is in kind of a class by itself. It has alpha-2 antagonist properties, but it's not a reuptake blocker. DR. LESLIE LUNDT: Now you mentioned the newest one on the market is desvenlafaxine or Pristiq. What do we need to know about that, that’s probably the one people are least familiar with? DR. STEPHEN M. STAHL: Well, it is active metabolite of one that the listeners probably do know very well venlafaxine. It turns out that Effexor or venlafaxine is actually metabolized into desvenlafaxine just sort of like its name sound like. The main difference is that when you take desvenlafaxine © 2021 ReachMD Page 2 of 5 itself, you are not dependent on their conversion of the parent compound into it and that makes the net action more noradrenergic. In other words, venlafaxine is a little less noradrenergic at the end of the SNRI than is desvenlafaxine. So it’s a little more noradrenergic, it’s a little more predictable. It has perhaps fewer drug interactions, but it is very similar to venlafaxine. DR. LESLIE LUNDT: So, may be a bit more like Cymbalta than Effexor, is that one way to think about it? DR. STEPHEN M. STAHL: Well yes, in terms of its pharmacology, both Cymbalta and Pristiq are more noradrenergic. Their so called claim to fame of Pristiq, which will require marketing for a while to see if it's true is that it seems to be able to be used without much titration at least for the first line treatment of the easier patients. Mostly, Cymbalta and Effexor require some titration. Whether that will be true or whether it will be an advantage is really what we will have to find out if the drug is used in the early months. DR. LESLIE LUNDT: Now iif you are jjust jjoiiniing our diiscussiion, you are lliisteniing to the Clliiniiciian''s Roundtablle on ReachMD, The Channell for Mediicall Professiionalls. I am Dr. Leslliie Lundt, your host, and wiith me today iis Dr. Stephen M. Stahll. We are diiscussiing the llatest iin antiidepressant treatment. Dr. Stahl in your book, you have talked about the TMM, that was the new one for me. What are they? DR. STEPHEN M. STAHL: Well, it’s a trimonoamine modulator and what I mean by that were trimonoamines, they are serotonin, norepinephrine, and dopamine, and what is a modulator, it's something that may act either indirectly on monoamines or work if you will more better in the presence of an antidepressant that directly changes monoamines. What I mean by that it’s a number of hormones like estrogen, like thyroid. These agents in themselves possibly have a little bit of antidepressant effect that’s controversial and certainly not established, but certainly in combination with antidepressants can boost or modulate the trimonoamines that the antidepressant is already boosting or modulating and so give you a further efficacy boost to the antidepressant action. Another one is lithium, by itself at least in unipolar depression is not that good of a antidepressant, but can boost regular antidepressants and modulate monoamines while it's doing that and the new kid on the block is the L-methylfolate, which is the centrally active form of the vitamin folate. It's sister product would be S-adenosyl-methionine or SAMe and other natural products that could fall in this category include things as varied as testosterone, vitamin D, and omega-3 fatty acids, so these things are not as well investigated, none of them are approved as a monotherapy, but by various mechanisms, which we could discuss, but they all do have a way of boosting monoamines and helping antidepressants boost them if you will more better. DR. LESLIE LUNDT: Certainly, these "natural" treatments have a huge appeal with our patients. I note for me SAMe you know had some great press about 10 years or so ago, we tried it, and I can't say I ever noticed anything from SAMe, but now L-methylfolate and omega-3 fatty acids are sort of the rage. Is there any downside to at least trying them? © 2021 ReachMD Page 3 of 5 DR. STEPHEN M. STAHL: I don't think so. Some people are cynical and say that the mechanism of action of these agents is that they bind to money receptors. DR. LESLIE LUNDT: (laughs) DR. STEPHEN M. STAHL: They may do that, but actually the one that I am kind of interested in <_____> now is L-methylfolate. It turns out that L-methylfolate is a precursor for a co-factor that makes monoamine synthesis called biopterin and by doing that it can make more serotonin, norepinephrine, and dopamine. If you don't have folate, you can become depressed and people, who are folate deficient tend to have high levels of homocysteine, and if you give L-methylfolate, the homocysteine level will come down and particularly if you haven’t responded to an antidepressant, those are excellent candidates to give L-methylfolate for.
Load more

Recommended publications
  • Beyond Monoamines Towards the Development of Novel Antidepressants Oltre Le Monoamine Al Fine Di Sviluppare Nuovi Farmaci Antidepressivi
    Original article • Articolo originale Beyond monoamines towards the development of novel antidepressants Oltre le monoamine al fine di sviluppare nuovi farmaci antidepressivi M. Fornaro1,2 1 Department of “Scienze della Formazione”, University of Catania, Italy; 2 Department of Psychiatry, Veteran Affairs (VA) Hospital, University of California (UCSD), La Hoya, San Diego, CA, USA Summary ated giving priority to RCTs and meta-analyses. At present, the pharmacological management of depression appears is Objective characterized by a wide variety of different augmentation or Herein, a concise review is presented on the current and most switching approaches (Fig. 1). Nonetheless, response rates promising antidepressant pharmacological agents for manage- remain substantially unsatisfactory, thus prompting for the ment of depression. development of novel agents with different mechanisms of action. Materials and methods A PubMed search (1966 - February 2012) was performed using Conclusions the following keywords or their combination: “depression”; Shifting the interest for novel antidepressant drugs beyond the “major depressive disorder”: “antidepressants”; “novel antide- monoaminergic modulation represents (Tables I-III) an intriguing pressant targets”; “monoamine”; “novel antidepressants”. Ad- opportunity to enhance response rates of depression, although ditional literature sources, including most authoritative and up- other issues, including revision of current nosological bounda- dated edited books or pamphlets were examined accordingly.
    [Show full text]
  • PHARMACEUTICAL APPENDIX to the TARIFF SCHEDULE 2 Table 1
    Harmonized Tariff Schedule of the United States (2020) Revision 19 Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE Harmonized Tariff Schedule of the United States (2020) Revision 19 Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 2 Table 1. This table enumerates products described by International Non-proprietary Names INN which shall be entered free of duty under general note 13 to the tariff schedule. The Chemical Abstracts Service CAS registry numbers also set forth in this table are included to assist in the identification of the products concerned. For purposes of the tariff schedule, any references to a product enumerated in this table includes such product by whatever name known.
    [Show full text]
  • National Horizon Scanning Centre Amibegron
    National Horizon Scanning Centre Amibegron (SR–58611) for depression April 2008 This technology summary is based on information available at the time of research and a limited literature search. It is not intended to be a definitive statement on the safety, efficacy or effectiveness of the health technology covered and should not be used for commercial purposes. The National Horizon Scanning Centre Research Programme is part of the National Institute for Health Research April 2008 National Horizon Scanning Centre News on emerging technologies in healthcare Amibegron (SR–58611) for depression Target group • Major depressive disorder (MDD). Technology description Amibegron is a selective beta 3-adrenoceptor, which stimulates neuronal activity in a specific area of the prefrontal cortex. Amibegron is an oral formulation administered at 175mg or 350mg twice daily. Innovation and/or advantages Amibegron is the first in a new class of antidepressant agents. It is anticipated that it will have less toxicity than current treatments. Developer Sanofi-Aventis. Availability, launch or marketing dates, and licensing plans: In phase III clinical trials. NHS or Government priority area: This topics relates to the National service framework for mental health: modern standards and service models. 19991. Relevant guidance • NICE technology appraisal. Depression and anxiety - Computerised cognitive behaviour therapy for depression and anxiety. 20062. • NICE clinical guideline in development. Depression - primary and secondary care: The treatment and management of depression in primary and secondary care. Expected June 20093. • NICE clinical guideline in development. Depression - chronic health problems: The treatment of depression in people with chronic physical health problems. Expected June 20094. • NICE clinical guideline.
    [Show full text]
  • Objectives Results Material-Methods
    v ANXIOLYTIC-LIKE EFFECT OF BETA RECEPTOR AGONIST AMIBEGRON (SR 58611A) WHICH MAY BE RELATED TO INTERACTION OF SEROTONIN RECEPTOR SUBTYPES 1 1 2 2 2 2 2 Pelin Tanyeri , Mehmet Emin Büyükokuroğlu , Oguz Mutlu , Güner Ulak , Füruzan Yıldız Akar , İpek Komşuoğlu Çelikyurt , Bekir Faruk Erden 1 Sakarya University, Faculty of Medicine, Department of Pharmacology, 54100-Sakarya/Turkey, 2 Kocaeli University, Faculty of Medicine, Department of Pharmacology, 41380-Kocaeli/Turkey OBJECTIVES THE AIM OF THE STUDY MATERIAL-METHODS Anxiety disorders are the most common and prevalent behavioral disorders with high comor- This study is aimed to investigate the effects of the first selective beta3 adrenergic agent ami- We used the serotonin 5HT1A receptor antagonist WAY-100635, serotonin 5HT2A-2C re- bidity rates. The decrease of the serotonergic activity and dysregulation of catecholaminer- begron on anxiety and also the involvement of different serotonin receptor subtypes in this ceptor antagonist ketanserin and serotonin 5HT3 receptor antagonist ondansetron in the ele- gic system may play a role in the pathogenesis of anxiety. effect. vated plus maze test. RESULTS CONCLUSION DISCLOSURE PANELS Amibegron (5 and 10 mg/kg) dose dependently prolonged the time spent in open arms and the number of entries to the open arms in mice EPM test. WAY, ketanserin and ondanset- In conclusion, amibegron exerted significant anxiolytic-like ef- Nothing to disclose ron had no effect on the time spent in open arms and the number of entries to the open arms in mice and also they all significantly reversed amibegron (10 mg/kg)-induced increase in fects in the mice EPM test which was as effective as diazepam.
    [Show full text]
  • The Use of Stems in the Selection of International Nonproprietary Names (INN) for Pharmaceutical Substances
    WHO/PSM/QSM/2006.3 The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances 2006 Programme on International Nonproprietary Names (INN) Quality Assurance and Safety: Medicines Medicines Policy and Standards The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances FORMER DOCUMENT NUMBER: WHO/PHARM S/NOM 15 © World Health Organization 2006 All rights reserved. Publications of the World Health Organization can be obtained from WHO Press, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland (tel.: +41 22 791 3264; fax: +41 22 791 4857; e-mail: [email protected]). Requests for permission to reproduce or translate WHO publications – whether for sale or for noncommercial distribution – should be addressed to WHO Press, at the above address (fax: +41 22 791 4806; e-mail: [email protected]). The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement. The mention of specific companies or of certain manufacturers’ products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.
    [Show full text]
  • GPCR/G Protein
    Inhibitors, Agonists, Screening Libraries www.MedChemExpress.com GPCR/G Protein G Protein Coupled Receptors (GPCRs) perceive many extracellular signals and transduce them to heterotrimeric G proteins, which further transduce these signals intracellular to appropriate downstream effectors and thereby play an important role in various signaling pathways. G proteins are specialized proteins with the ability to bind the nucleotides guanosine triphosphate (GTP) and guanosine diphosphate (GDP). In unstimulated cells, the state of G alpha is defined by its interaction with GDP, G beta-gamma, and a GPCR. Upon receptor stimulation by a ligand, G alpha dissociates from the receptor and G beta-gamma, and GTP is exchanged for the bound GDP, which leads to G alpha activation. G alpha then goes on to activate other molecules in the cell. These effects include activating the MAPK and PI3K pathways, as well as inhibition of the Na+/H+ exchanger in the plasma membrane, and the lowering of intracellular Ca2+ levels. Most human GPCRs can be grouped into five main families named; Glutamate, Rhodopsin, Adhesion, Frizzled/Taste2, and Secretin, forming the GRAFS classification system. A series of studies showed that aberrant GPCR Signaling including those for GPCR-PCa, PSGR2, CaSR, GPR30, and GPR39 are associated with tumorigenesis or metastasis, thus interfering with these receptors and their downstream targets might provide an opportunity for the development of new strategies for cancer diagnosis, prevention and treatment. At present, modulators of GPCRs form a key area for the pharmaceutical industry, representing approximately 27% of all FDA-approved drugs. References: [1] Moreira IS. Biochim Biophys Acta. 2014 Jan;1840(1):16-33.
    [Show full text]
  • Using Tests and Models to Assess Antidepressant-Like Activity in Rodents Ewa Kedzierska1*, Izabela Wach2
    DOI: 10.1515/cipms-2016-0013 Curr. Issues Pharm. Med. Sci., Vol. 29, No. 2, Pages 61-65 Current Issues in Pharmacy and Medical Sciences Formerly ANNALES UNIVERSITATIS MARIAE CURIE-SKLODOWSKA, SECTIO DDD, PHARMACIA journal homepage: http://www.curipms.umlub.pl/ Using tests and models to assess antidepressant-like activity in rodents Ewa Kedzierska1*, Izabela Wach2 1 Chair and Department of Pharmacology and Pharmacodynamics, Medical University of Lublin, Chodzki 4A, 20-093 Lublin, Poland 2 Student Research Group at the Chair and Department of Pharmacology and Pharmacodynamics, Medical University of Lublin, Chodzki 4A, 20-093 Lublin, Poland ARTICLE INFO ABSTRACT Received 08 February 2016 In today's world, depression is one of the more prevalent forms of mental illness. According Accepted 10 March 2016 to WHO, about 10%-30% of all women and 7%-15% of all men are afflicted by depression Keywords: at least once in their life-times. Today, depression is assessed to be affecting 350 million depression, people. Regarding this issue, an important challenge for current psychopharmacology animal models, is to develop new, more effective pharmacotherapy and to understand the mechanism atidepressants. of action of known antidepressants. Furthermore, there is the necessity to improve the effectiveness of anti-depression treatment by way of bringing about an understanding of the neurobiology of this illness. In achieving these objectives, animal models of depression can be useful. Yet, presently, all available animal models of depression rely on two principles: the actions of known antidepressants or the responses to stress. In this paper, we present an overview of the most widely used animal tests and models that are employed in assessing antidepressant-like activity in rodents.
    [Show full text]
  • Datasheet Inhibitors / Agonists / Screening Libraries a DRUG SCREENING EXPERT
    Datasheet Inhibitors / Agonists / Screening Libraries A DRUG SCREENING EXPERT Product Name : Amibegron hydrochloride Catalog Number : T10302 CAS Number : 121524-09-2 Molecular Formula : C22H27Cl2NO4 Molecular Weight : 440.36 Description: Amibegron hydrochloride is a selective β3-adrenoceptor agonist (EC50: 3.5 nM for β-adrenoceptor in rat colon). It has anxiolytic and antidepressant activity. Storage: 2 years -80°C in solvent; 3 years -20°C powder; Receptor (IC50) β-adrenoceptor 499 nM In vitro Activity Amibegron hydrochloride (SR 58611A) is a selective β-adrenoceptor agonist (EC50: 499 nM in rat uterus) [1]. Amibegron hydrochloride shows little effect on β1- and β2-adrenoceptors, 5-HT uptake, noradrenaline (NA) uptake, and dopamine (DA) uptake from rat brain tissue (IC50s: 4.6 and 1.2, 0.58, 2.5 and 3.2 μM). It exhibits no effect on 5-HT1A, 5-HT2, MAO-A, and MAO-B (IC50 > 10 μM) [2]. In vivo Activity Amibegron hydrochloride (0.1 to 0.3 mg/kg, i.p.) potentiates the toxicity produced by yohimbine in mice. Amibegron hydrochloride (0.6 and 2 mg/kg, i.p.) is also active in the learned helplessness model of antidepressant-like activity in rats [2]. Amibegron hydrochloride (3 and 10 mg/kg, p.o.) increases the synthesis of 5-HT and tryptophan (Trp) levels in several rodent brain areas such as cortex, hippocampus, hypothalamus. In addition, Amibegron hydrochloride (10 mg/kg, p.o.) promotes the release of 5-HT in the rat prefrontal cortex. Systemic (3 mg/kg, i.v.) or chronic administration of SR58611A (10 mg/kg, p.o.) does not affect the activity of serotonergic neurons in the rat dorsal raphe nucleus [3].
    [Show full text]
  • Impact of Depressogenic- and Antidepressant-Like
    Impact of depressogenic- and antidepressant-like challenges on monoamine system activities: in vivo electrophysiological characterization studies Chris A. Oosterhof Department of Cellular & Molecular Medicine University of Ottawa Thesis submitted in partial fulfillment of the requirements for the Doctor of Philosophy Degree in Neuroscience © Chris A. Oosterhof, Ottawa, Canada, 2016 Table of contents Table of contents ............................................................................................................. ii Acknowledgements ........................................................................................................ iv Statement of contributions .............................................................................................. v List of figures ................................................................................................................. vi List of tables .................................................................................................................. vii Glossary ........................................................................................................................ viii Abstract .......................................................................................................................... xi 1) Major depressive disorder ............................................................................................... 1 2) Monoamine systems.......................................................................................................
    [Show full text]
  • PHARMACEUTICAL APPENDIX to the TARIFF SCHEDULE 2 Table 1
    Harmonized Tariff Schedule of the United States (2011) Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE Harmonized Tariff Schedule of the United States (2011) Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 2 Table 1. This table enumerates products described by International Non-proprietary Names (INN) which shall be entered free of duty under general note 13 to the tariff schedule. The Chemical Abstracts Service (CAS) registry numbers also set forth in this table are included to assist in the identification of the products concerned. For purposes of the tariff schedule, any references to a product enumerated in this table includes such product by whatever name known.
    [Show full text]
  • Фармакология Pharmacology
    МИНИСТЕРСТВО ЗДРАВООХРАНЕНИЯ РЕСПУБЛИКИ БЕЛАРУСЬ БЕЛОРУССКИЙ ГОСУДАРСТВЕННЫЙ МЕДИЦИНСКИЙ УНИВЕРСИТЕТ КАФЕДРА ФАРМАКОЛОГИИ ФАРМАКОЛОГИЯ PHARMACOLOGY Практикум для специальности «Лечебное дело» 5-е издание, переработанное Минск БГМУ 2020 2 УДК 615(076.5)(075.8)-054.6 ББК 52.81я73 Ф24 Рекомендовано Научно-методическим советом университета в качестве практикума 29.05.2020 г., протокол № 9 А в т о р ы: проф. Н. А. Бизунок, проф. Б. В. Дубовик, доц. Б. А. Волынец, доц. А. В. Волчек Р е ц е н з е н т ы: д-р мед. наук, проф. А. В. Хапалюк; д-р. мед. наук, проф. А. И. Волотовский Фармакология = Pharmacology : практикум для специальности «Лечебное дело» / Ф24 Н. А. Бизунок [и др.]. – 5-е изд., перераб. – Минск : БГМУ, 2020. – 156 с. ISBN 978-985-21-0643-6. Содержит методические рекомендации для подготовки к лабораторным занятиям по фармакологии и задания для самостоятельной работы студентов, обучающихся по специальности 1-79 01 01 «Лечебное дело». Первое издание вышло в 2016 году. Предназначен для студентов 3-го курса медицинского факультета иностранных учащихся, изучающих фармакологию на английском языке. УДК 615(076.5)(075.8)-054.6 ББК 52.81я73 ISBN 978-985-21-0643-6 © УО «Белорусский государственный медицинский университет», 2020 3 CONTENTS INTRODUCTION ............................................................................................................................................................. 4 GENERAL PRESCRIPTION ...........................................................................................................................................
    [Show full text]
  • 5-HT2A Receptors in the Central Nervous System the Receptors
    The Receptors Bruno P. Guiard Giuseppe Di Giovanni Editors 5-HT2A Receptors in the Central Nervous System The Receptors Volume 32 Series Editor Giuseppe Di Giovanni Department of Physiology & Biochemistry Faculty of Medicine and Surgery University of Malta Msida, Malta The Receptors book Series, founded in the 1980’s, is a broad-based and well- respected series on all aspects of receptor neurophysiology. The series presents published volumes that comprehensively review neural receptors for a specific hormone or neurotransmitter by invited leading specialists. Particular attention is paid to in-depth studies of receptors’ role in health and neuropathological processes. Recent volumes in the series cover chemical, physical, modeling, biological, pharmacological, anatomical aspects and drug discovery regarding different receptors. All books in this series have, with a rigorous editing, a strong reference value and provide essential up-to-date resources for neuroscience researchers, lecturers, students and pharmaceutical research. More information about this series at http://www.springer.com/series/7668 Bruno P. Guiard • Giuseppe Di Giovanni Editors 5-HT2A Receptors in the Central Nervous System Editors Bruno P. Guiard Giuseppe Di Giovanni Faculté de Pharmacie Department of Physiology Université Paris Sud and Biochemistry Université Paris-Saclay University of Malta Chatenay-Malabry, France Msida MSD, Malta Centre de Recherches sur la Cognition Animale (CRCA) Centre de Biologie Intégrative (CBI) Université de Toulouse; CNRS, UPS Toulouse, France The Receptors ISBN 978-3-319-70472-2 ISBN 978-3-319-70474-6 (eBook) https://doi.org/10.1007/978-3-319-70474-6 Library of Congress Control Number: 2017964095 © Springer International Publishing AG 2018 This work is subject to copyright.
    [Show full text]